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Showing posts with label inferior wall. Show all posts
Showing posts with label inferior wall. Show all posts

Tuesday, April 5, 2016

Way Too Overdue: Subtle STEMIs and Stubborn Platelets March 2016 PART 1/2


SUBJECTIVE:

EMS responds to the report of a 48 yo female with chest pain. Upon arrival, the patient is in mild distress and reports sharp, intermittent, right sided chest discomfort lasting for approximately 30 minutes. The patient reports nausea, some slight diaphoresis, and denies vomiting. The patient reports recent intake of cocaine and has a history of substance abuse. The patient has no allergies.

PMHX:
HIV
HTN

OBJECTIVE: 
The patient is awake, alert, oriented, and seated in a chair. BP: 160/100, P: 80, R: 72. Sp02: 97% on RA. Lungs are clear to auscultation bilaterally. Heart sounds are regular. The abdomen is soft and the remainder of the physical assessment is unremarkable. Peripheral pulses are strong and equal.

A 12 lead ECG is obtained:

What's your interpretation and treatment plan? 
An intravenous line is started.

Thursday, April 23, 2015

April 2015: Sighting the Subtlety Down Below



CASE: 

A 63 y/o gentleman calls 911 for "chest pressure" and indigestion. The patient is nauseated but denies LOC, SOB, or dizzinesss. The pressure started approximately 1 hour prior to 911 arrival. The patient has a history of hypertension and takes an aspirin daily. He is hemodynamically stable. BP is 110/70, P: 82, R: 16. Sp02: 95% on RA.

12 LEAD ECG:
























12 LEAD ECG DISCUSSION:

There is a sinus rhythm. PR depression is present in lead II. There is slight ST segment elevation present in II, III, and aVF. Elevation measures about 1 mm. There is no evidence of recriprocal change. A biphasic T wave is present in lead III and terminal T wave inversion is present in the lateral precordial leads. The QRS axis appears physiologic.

12 LEAD INTERPRETATION: 

Inferior wall STEMI

TREATMENT

The patient was transported to a hospital capable of percutasneous coronary intervention. A right sided ECG was not performed, and NTG was withheld due to the patient's marginal blood pressure or relative hypotension. 325 mg of ASA was administered. The patient's RCA was 75% occluded.

Thanks always to the Baltimore City Fire Department for its endless supply of pathologic 12 lead tracings.

Sunday, August 31, 2014

August 2014: Right behind you with a STEMI!

A 60 yo male patient reports a sudden onset of chest pain and shortness of breath. The patient rates the pain at an 8/10 and is slightly nauseated. The patient has a history of "borderline" diabetes.

VS:
BP: 140/90, P: 62, R: 16, Sp02: 99%

EXAM:
The patient is slightly diaphoretic and appears uncomfortable. A 12 lead ECG is obtained.

ACTIONS:Do you activate the cath lab?
Do you administer NTG?

12 LEAD ECG: 


12 LEAD ECG CASE DISCUSSION:

The ECG shows a first degree heart block. ST segment elevations are apparent in Leads II, III, and aVF. Reciprocal changes are present in Leads I and aVL. ST segment changes are present in the septal leads of V3 to V4. The diagnosis of a posterior wall myocardial infarction is less likely given (1) the absence of tall R waves and (2) The absence of ST depression in leads V1-V3. However, anytime anterior precordial ST depression appears concurrently with an inferior wall MI, you should consider the diagnosis of a posterior wall infarction. Recall that the posterior descending coronary artery comes from the right coronary artery. It is wise to be cautious with nitroglycerin since this infarction may involve portions of the right ventricle. Have IV access established and consider right sided chest leads if there is concern for a right ventricular infarction. This patient went emergently to the cardiac catheterization lab and was found to have a completely (100%) occluded right coronary artery.  Finally, conduction delays and heart blocks are consistent with ischemia of the sinoatrial node and the conduction system.

12 LEAD ECG INTERPRETATION:
Inferior wall ST elevation myocardial infarction.

Thursday, May 22, 2014

Pointy ST Segments and Abnormal Labs

Your crew responds to a local skilled nursing facility for a patient with "abnormal labs." The nurse tells you that the patient's "K was elevated." The patient reports a near syncopal episode approximately 40 minutes prior to arrival. The patient feels weak and dizzy. No chest pain, shortness of breath, or vomiting is endorsed. The patient is ill appearing but awake, alert, and oriented.

Vital signs:
BP: 82/40
P: 49
R: 16
Sp02: 86% on room air


A 12 lead ECG is obtained:



12 Lead ECG Discussion

The rhythm is sinus bradycardia. Unless this 80 year old is a marathon runner, the rate is abnormal. Furthermore, the bradycardia occurs in association with (1) near syncope and (2) abnormal vital signs. ST segment elevation is seen in leads II, III, and aVF. Reciprocal change in the form of ST segment depression is seen in lead aVL. STE is also observed in the lateral precordial leads. The R waves are tall in V2 and V3 but there is no concurrent ST segment depression to suggest involvement of the heart's posterior wall. Q waves, though not pathologic, appear in leads II, III, and aVF, and favor the diagnosis of ischemia.

12 Lead ECG Interpretation 

Sinus bradycardia, Inferior-lateral ST segment myocardial infarction. 

Case Discussion

This case presents more than a few dilemmas and teaching points. First, it emphasizes the association between dizziness, weakness, and acute coronary syndromes. Elderly patients may not present with the classic "chest pain" or "chest pressure." Dyspnea, dizziness, and weakness are well known anginal equivalents and should be aggressively investigated, especially in the setting of abnormal vital signs. The presence of peaked T waves might suggest underlying hyperkalemia. The changes associated with hyperkalemia are usually diffuse. The STE in this ECG follows an anatomic (inferior-lateral) pattern. If there is concern for "abormal labs," then the administration of calcium is probably warranted. Calcium should always be considered first line in the management of hyperkalemic emergencies.

What About the Rate? 

This patient also presents with symptomatic bradycardia. A well accepted axiom in EMS and emergency medicine is, "fix the rate FIRST." EMS protocols would probably advocate for a healthy dose of atropine. Ischemia of the SA node (caused by RCA occlusion) can certainly result in a symptomatic bradycardia, heart blocks, and other types of badness. However, be cautious when administering atropine to a patient suffering from an active MI. Atropine will increase myocardial demand and have the potential to exacerbate ischemic symptoms. A gentle fluid bolus may suffice to mitigate hypotension, and opening of an occluded RCA will make everything right as rain...

KEY POINTS:
  • Fix the rate first (WITH CAUTION in cases of active ischemia!) 
  • Calcium is first line in the treatment of suspected hyperkalemia and ECG changes
  • Weakness, dizziness, and syncope should be regarded as anginal equivalents- especially in the elderly 
  • Inferior wall myocardial infarction can produce bradycardia, heart blocks, and syncope
Special thanks to JoElyn for providing these ridiculously complex ECGs! (And best wishes as a newly minted registry medic...) 

Sunday, August 11, 2013

Look Behind You!

A 45 yo female with a history of cigarette smoking and tobacco abuse reports a sudden onset of severe, substernal chest discomfort. EMS providers perform a 12 lead ECG.







12 Lead Discussion

ST elevation is noted in leads II, III, and aVF. Reciprocal changes are seen in leads I and aVL. Note ST elevation extends into the lateral precordial leads of V4, V5, and V6. Also of significance is the ST segment depression in leads V2 and V3. Though the R waves aren't especially tall, the ST depression and slightly positive R waves is consistent with extension of the infarction into the heart's posterior wall. A large obstructing lesion of the right coronary artery can affect these geographic areas of the heart. Posterior wall MIs usually do not occur in isolation. The "Life in the Fast Lane" blog has a good page on the interpretation of the posterior wall myocardial infarction. 

12 Lead Interpretation

Inferior lateral ST elevation myocardial infarction with extension into the posterior wall.

Tuesday, April 9, 2013

Where is the Circulatory Road Block?

Case

An 81 y/o female with DM, HTN, and bilateral lower extremity amputations presents to EMS with chest pain and vomiting. VS: BP: 90/40, P: 80, R:16. Sp02: 95%. The patient is alert and oriented and in mild distress. An ECG is obtained. What is your interpretation ?

12 Lead ECG




ECG Interpretation 

A first degree AV block is present. Deep Q waves and ST elevations are present in the inferior leads III, and aVF. Additional ST segment elevations are present in the anterior precordial leads V3, V4, and V5. Reciprocal depression is present in leads I and aVL. A right bundle branch block is suggested by the positively deflected QRS and increased QRS duration seen in V1. This patient is experiencing a large STEMI given the presence of elevation in multiple territories. ST elevations suggest active injury and ischemia in the inferior and anterior leads. The relative hypotension may indciate cardiogenic shock. Cardiogenic shock complicates a significant percentage of anterior wall myocardial infarctions. Multi-territorial ST elevations indicates a poor prognosis.

Treatment Course 

Providers transmit the 12 lead ECG and alert the receiving facility of an ST elevation myocardial infarction. Aspirin is administered. The patient proceeds directly to the cath lab. The patient had severe, multi-vessel, obstructive coronary artery disease and unfortunately expired from decompensated cardiogenic shock

Key Points


  • Remain vigilant for the presence of cardiogenic shock in the presence of anterior wall ischemia
  • ST elevations in multiple geographic areas (inferior and anterior in this case) indicate severe disease
  • Ventricular fibrillation can also accompany large anterior wall MIs
  • Relative hypotension is extremely significant in patients who are accustomed to higher blood pressures. In this case, the patient's marginal blood pressure resulted from acutely decreased cardiac output. 




Saturday, December 8, 2012

Simply a Sinus STEMI? No!

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Paramedics respond to a 55 yo female with chest pain and shortness of breath. The patient is alert and hypertensive. The peripheral pulse is irregular.

12 lead ECG: 


12 Lead ECG Interpretation:

The underlying rhythm is most definitely not sinus. A rhythm strip is not included in the LifeNet transmission. Though the first visualized QRS complex in leads I, II, and III APPEARS to be conducted, there is PR interval is excessively long (> 0.2seconds). Furthermore, the P to P intervals appear constant. There is a "p" hiding in the ST segment of the next QRS complex. The constant P to P interval suggests a third degree heart block. ST segment elevation is present in the inferior leads. Reciprocal change is evident in the anterior-septal (V1-V6) and lateral (I, aVL) leads. Recall that ST depression in the septal leads (V1-V2) could indicate posterior involvement. Posterior wall changes generally exhibit tall R waves in leads V1-V3 which are absent in this particular tracing. 


Third degree heart block, inferior wall ST segment myocardial infarction with possible posterior extension. 

12 lead ECG Case Discussion:

This case highlights the importance of a rhythm strip. If there is any question about the presence or absence of an underlying conduction problem, always obtain a rhythm strip. LifeNet provides just a few seconds of rhythm analysis; this interval is occasionally inadequate for proper rhythm determination. Inferior wall changes, coupled with the heart block, suggest injury to the SA node. This patient would benefit from the prophylactic application of pacing pads. Avoid nitrogylcerin in the presence of inferior wall changes and an underlying heart block. 

The "buried P wave" and constant P to P interval: 
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Thursday, May 24, 2012

"Abnormal ECG" and Bypass of the Closest Facility

So.. would you call this one and activate the cath lab from the prehospital ECG? The patient is a 72 year old female with severe uncontrolled hypertension. She called 911 for mild shortness of breath. Her blood pressure is over 200 mm Hg systolic. The patient is awake, alert, and oriented. The paramedic is bypassing a local facility in favor of the closest cardiac interventional center.

What's your analysis?

12 Lead ECG

 

12 Lead ECG Interpretation and Discussion

A baseline sinus rhythm is present. There is a significant amount of artifact that interferes with interpretation in the limb leads. A fusion beat is seen in the limb lead tracings. However, there is > 1mm of ST segment elevation in lead III. Lead aVF also has minimal ST segment elevation. Pathologic Q waves are present in contiguous leads (III and aVF). Though an isolated Q wave is common in limb lead III, the presence of Q waves in contiguous inferior leads (III and aVF) suggests ischemia. In addition, ST segment depression is present in the reciprocal leads of I and aVL. This finding further supports the presence of acute injury. ST segment elevations are also seen in leads aVR and V1. As discussed in a previous case, the presence of STE in leads aVR and V1 may predict obstruction of the left main coronary artery. Poor R wave progression is present across the precordial leads V2-V6. This finding  (the loss of R wave amplitude) is consistent with the machine generated diagnosis of "anterior infarct, age undetermined." These findings, when put together, reveal an inferior wall STEMI. This patient is best cared for at a facility capable of percutaneous cardiac intervention.

Final interpretation

Sinus rhythm, inferior wall STEMI. Anterior wall ischemia. Reciprocal changes in the form of ST depression present in the anterior-lateral limb leads.


Tuesday, March 13, 2012

The Bottom Line: NTG and ECG

A patient walked into the triage area and reported chest pain, nausea, and "indigestion" for several hours. Initial vitals were stable. After a dose of nitroglycerin, the patient's "stable" vital signs had left the building. Though conscious, a repeat set of vitals (following the NTG dose) was as follows:
BP: 76/40
(Taken mutiple times on multiple extremities)
P: 72
Sp02: 89%
The hypotension resolved after a fluid bolus. An ECG finding (conveniently circled by an alert resident) reveals the answer to the hypotension story..

Right Sided 12 LEAD ECG

12 LEAD ECG INTERPREATION AND DISCUSSION

A baseline sinus rhythm is present. ST segment elevations are seen in the inferior wall leads II, III, and aVF. Expected reciprocal changes in the form of ST segment depressions are seen in leads I and aVL. The right sided chest lead V4 (V4R)  shows ST elevation. STE in V4R indicates right ventricular infarction. These patients are preload dependent. Nitroglycerin is a potent vasodilator. When this drug is administered in the setting of a right ventricular infarction, it can cause significant hypotension. The precipitous drop in blood pressure usually resolved after a fluid bolus.

PEARLS
  • Initiate IV access prior to nitroglycerin administration in patients with inferior wall changes
  • Look for right ventricular myocardial infarction by obtaining right sided chest leads
  • Right ventricuar infarction usually co-exists with inferior wall ischemia
  • STE in II, III, aVF ? Start an IV and reassess folliwing NTG administration!